Presents Dr. E. Barrie Kenney Professor & Chairman Section of Periodontics
E. Barrie Kenney B.D.Sc., D.D.S., M.S., F.R.A.C.D.S.Tarrson Family Endowed Chair in Periodontics.Professor and Chairman Division of AssociatedClinical Specialties UCLA School of Dentistry
Many clinicians believe Traumaticocclusion causes IntrabonyPeriodontal defects but this is not so.This defect is caused by dental plaquewith accentuation due to the opencontact region and poor subgingivalmargin of Restoration.
Histology of Intrabony defect dueto plaque induced Periodontitis.Arrows show sub gingival plaqueon root surface
Irritation factors are plaque thatinduces Gingivitis whichprogresses to Periodontitis.Traumatizing factors fromocclusion cause tissue changes inperiodontal ligament space.
Zone of co-destruction occurs whenplaque induced Periodontitis occurs ina tooth that also has TraumaticOcclusion resulting in more severebone loss than that seen withPeriodontitis alone.
Host parasite reaction betweenbacterial plaque and hostinflammatory response is the causeof pocket depth and attachment loss.The presence of Traumatic occlusioncan accentuate the damage whenPeriodontitis proceeds apically intothe Periodontal Ligament Space.
The first reaction to increasedTissue Changes Due to occlusal loading is increased vascularity in the Periodontal Traumatic Occlusion ligament space. No changes are seen in gingival tissues.
Normal Periodontal ligamentwith normal occlusal forcesshowing dense collagen fibersattached to bone andcementum with minimalvascularity.
With excessive occlusalloading the collagen fibers losetheir connections betweencementum and bone ,andblood vessels proliferate.
This initial increasedvascularity results in a morecompressible periodontalligament and increased clinicalmobility.
Changes in the apicalperiodontal ligament vascularpatterns can also result inincreased vasodilation of thepulp with increased sensitivityand pain to Hot and Coldstimuli secondary to TraumaticOcclusion.
In Traumatic Occlusion afterthe initial change of increasedvascularity, there is astimulation of osteoclastswhich cause bone loss and awidened periodontal ligamentspace. This also causesincreased tooth mobility.
Further effects of TraumaticOcclusion are seen with loss of Loss of Density ofdensity of collagen and Collagenabsence of a functional fiberarrangement.
High power view. No collagenfibers adjacent to bone andloss of functional support ofPeriodontium.
Normal Periodontium Result of Traumatic Occlusion
Periodontal ligament tissuescan respond with Traumatic These changes are calledOcclusion changes when a Primary Occlusal Trauma ornormal periodontium is Primary Trauma fromaffected by increased occlusal occlusion.loading due to bruxingclenching or a high restoration
In teeth with bone loss due toperiodontal disease previously These changes are calledwell tolerated occlusal loading secondary occlusal trauma orcan become traumatic and secondary trauma fromcause changes in the occlusion.periodontal ligament tissues.
Coronal portion of plaqueinduced Periodontitis withpocket formulation
Region of crestal bone showingintrabony pocket due toplaque this is blending withTraumatic Occlusion inducedPeriodontal ligament changesof loss of collagen andincreased vascularity.
More Apical region withTraumatic Occlusion changesseen deep in Periodontaltissues apical to Periodontitis.
Apical part of Traumticplaque induced occlusion Periodontitis changes deep in periodontal ligament
Radiograph of lower Molar withTraumatic Occlusion. WidenedPeriodontal ligament space onMesial all the way around theapex with beginning bone lossin furcation (arrows).
There is also thickened laminadura and this tooth hasincreased mobility.
First molar has traumatic occlusioncausing the bone loss in the furca.Clinically there is no pocket depthnor Periodontitis in the furcationand so the diagnosis is TraumaticOcclusion and the treatment isocclusal adjustment to reduceocclusal loading.
Both premolars have traumaticocclusion and there is anaddition Periodontitis relatedbone loss and pockets on themesial of the first premolar.
Gingival recession is notcaused by Traumatic Occlusionbut is related to inadequateKeratinized Gingiva andexcessive tooth brushing.
Wedge shaped defect in rootof lower first premolar is dueto traumatic toothbrushingand is not related to TraumaticOcclusion
“Abfraction” type of root losslike this has not been shownto occur clinically inassociation with heavy occlusalforces.
At time of Periodontal surgerylarge hyperplastic boneresponse to heavy occlusalload called Buttressing Bone
Buttressing Bone removedduring periodontal surgery tofacilitate normal contour ofgingival tissues.